To further validate the relationship between them, the accelerated proliferation and reduced apoptosis induced by ECT2 overexpression were negated by the transfection of si-AKT into ECT2-overexpressing cervical cancer cells; These results suggest that the downregulation of AKT can reverse the anti-apoptosis, proliferation and activation of the AKT/mTOR pathway induced by ECT2 overexpression, and further reveal that ECT2 promotes the malignant progression of cervical cancer by regulating the AKT/mTOR pathway (Sharma et al., 2012). This evidence concerns the gene AKT1 and cervical carcinoma.